Search bioRxiv⌕ Search

Biology subjects

Meyerink, M.

Publications and source records attributed to Meyerink, M..

2 recordsLinked to original sources

Fat body driver expression report across Drosophila melanogaster tissues and sex

Drosophila melanogaster serves as a valuable model system for advancing our understanding of adipose tissue given its analogous organ systems, conserved metabolic, endocrine, and nutrient-sensing functions, and well-established genetic tools. Among the most widely used genetic tools is the Gal4/UAS system. Several Gal4 driver lines are reported to control expression in the D. melanogaster fat body, but secondary expression sites and responses to physiological changes have not been fully characterized. In this report, we describe fluorescent reporter expression for 31 fat body Gal4 transgenic lines in larvae and adults, males and females, and in multiple tissues, brain, indirect flight muscle, gut, ovary, testis, and fat body. This screen highlights expression differences with respect to level, sex, and stage. Moreover, we find that several lines drive expression in tissues that had not been previously described. Together, we present a comprehensive expression atlas of fat body driver lines, serving as a resource to advance adipose tissue research.

cell biology↗

DUSP5 Downregulation in Nucleus Accumbens Core Correlates with Synaptic Plasticity and Cue-Induced Cocaine Reinstatement

The United States is currently facing a drug overdose epidemic, with substance use disorder (SUD) characterized by cyclical phases of drug use, withdrawal, and relapse. The nucleus accumbens core (NAcore), a brain region critical for reward and aversion behaviors, undergoes structural and functional synaptic adaptations in response to chronic drug exposure. These changes, particularly in dopamine D1 receptor-expressing medium spiny neurons (D1-MSNs), are implicated in drug-seeking behaviors and synaptic plasticity. However, the molecular mechanisms underlying these adaptations remain poorly understood. In this study, we investigate the role of dual-specificity phosphatase 5 (DUSP5), an phosphatase known to deactivate extracellular signal-regulated kinase (ERK), in cocaine-induced neuroplasticity. While prior research has linked other DUSP family members to various drugs of abuse, the specific role of DUSP5 in cocaine addiction remains unexplored. We hypothesized that lack of DUSP5 contributes to NAcore synaptic plasticity during cue-induced cocaine reinstatement. To test this, we employed a rat cocaine self-administration model, integrated molecular analyses, and mined publicly available single-cell RNA sequencing data from cocaine-treated NAcore. Our findings aim to elucidate the potential involvement of DUSP5 in cocaine-related synaptic adaptations and behavior, addressing a significant gap in the mechanistic understanding of SUD.

neuroscience↗